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Flashcards in Week 13: Acute GI dysfunction Deck (65):

upper GI type of bleeding?

arterial, hematemesis and melena


lower GI type of bleeding?

venous bleeding, hematochezia


Hematemesis bright and dark

bright: upper, higher up
darker: old bleed from jejunum where bile is breaking it down



-black tarry stool
-foul smelling, black (can happen only with 50 cc of bleeding)
-from small or ascending colon



-bright blood in stool=lower GI blood (from colon)


clinical manifestation of GI bleed

hematemesis, melena, hematochezia, fatigue, dyspnea, syncope, angina


Most common cause of upper GI bleeding

peptic ulcer disease


peptic ulcer disease

Causes: NSAIDS,H. Pylori, cigarette smoking
Types: Duodenal and gastric
Dx: H. pylori testing, visualization with endoscopy, barium x-ray, combination antibiotic (amoxy, clarithromycin, tetracycline, and metronidazole)
Treatment: H2 blockers, PPI


Acute erosive or hemorrhagic gastritis

-Severe inflammation of the gastric mucosa (NSAID gastritis, alcohol gastritis, stress gastritis)
-treatment: endoscopic sclerotherapy (inject something to make varices coagulate), vasopressin IV or intraarterial


esophageal and gastric varices

-associates with cirrhosis, portal htn, and portal or splenic vein thrombosis
-massive bleeding
-treatement: sclerotherapy or esophageal balloon (creates pressure to stop bleeding), can also band the verice or pollup
-this is often how end stage hepatic pts die


mallory-weiss tears

-a small tear in the mucosal lining at the gastro-esophageal junction (often preceded by vomit, most bleeds stop without intervention)
-DX with endoscopy
-If bleeding is excessive may treat with vasopressin, usually stops on its own


acute lower GI bleeds

Causes: diverticular bleeding, ischemic bowel disease, inflammatory bowel disease, neoplasms


Diverticular bleeding

-only occurs in about 3% of those with diverticulosis
-when occurs, may have massive loss of blood that is life threatening
-artery ruptures to fill diverticula
-dx with colonoscopy to determine reason for bleeding
25% require surgical intervention to stop bleed


ischemic bowel disease

-interruption of colonic blood supply (bowel obstruction, occlusion of blood flow through vascular system)
-risk factors: surgical procedure to vasculature and bowel resection, afib, atherosclerosis, hypotn, sickle cell, DM, lupus, pacreatitis, anticoagulant therapy
-S/S:* intermittent bleeding*. A pt. who's h&h is dropping and we don't know why, mixed dark and bright red bleeding, fever, abd pain
-DX: endoscopy shows purple color bowel, xray may show air sacks, barium contrast shows thumbprints
-TX: fix blood flow to bowel (fluid resuscitation), Antibiotic tx for infection, bowel resection as needed to remove necrotic bowel


inflammatory bowel disease

-S/S: bloody diarrhea, light to moderate bleeding
-TX: Stop bleeding, administration of corticosteroids to control inflammation, anti-TNF tx (immune biologic therapy), surgical resection as needed


what is anti-TNF used for

helps with inflammation in IBS, it is an immune biologic therapy



-up to 20% benign and malignant tumors are associated with bleeding
-slow, chronic, and self-limiting
-DX: barium x-rays, ct scan, mri, pet scan, endoscopy
-TX: dependent on type, stage, patient wishes


management of acute GI bleeding unstable pt.

-is the patient stable? (hypotn, tachy, altered LOC, cap refill delayed= unstable)
-urgent interventions: hemodynamic resuscitation and oxygen delivery
-establish cause of the bleeding once stabilized
-Is it upper or lower?
-Upper: hematoemesis and melana
-Lower: hematochezia (bright)


management of acute GI bleeding stable pt.

-stable? (bloody diahrrea, bp normal, AO=stable)
-Look at labs, get a really good history, meds (NSAIDS), alcohol consumption, cigarette smoking, sickle cell, clotting factor disorders
-is it upper or lower


initial assessment of GI bleed

Laboratory changes
-BUN/Creat (helps differentiate upper and lower. If greater than 35 think upper GI, less than 35 is probably lower GI)
-liver functions test
-cardiac enzymes (might be getting ischemic to heart muscle itself bc of blood loss)
-every pt. who comes in with GI bleed should be typed and crossed

Fluid Volume Status
-hypotension (SBP less than 90)
-narrowed pulse pressure (MAP less than 60)
-orthostatic hypotension (concerned with drop in BP 20mmhg or rise in HR of 20bp/min)
-ST changes (only when the pt is becoming ischemic. Need tele monitor)
-cap refill delayed
-mucous membranes dry
-UO dropping below 30cc/hr
-mental status changes


interventions in GI bleed

-Maximized 02 carryping capacity, keep 02 sat above 92%
-restore normovolemia: 2 large bore lvs, administer 2 liters of crystalloids (LR, normal saline, should see improvement in 20min), followed by PRBCs as needed, FFP, Platelets, Factor VIII
-Patient positioning to maintain SBP
-NG tube placement
-Erythromycin 3mg/kg over 20 minutes one hour prior to procedures
-Reglan 10 mg IV
-Bowel Prep


what guage in a pt. going to surgery or hemodynamically unstable

18 gauge


if hemoglobin is less than 7, then?

give blood no matter what, even if they have had a fluid challenge


If they are anticoagulated, and their PT is going to be greater than 13, and INR greater than 1.5, you are going to give them?

-FFP or platelets (provider preference)


Platelets less than 5,000 or after 10 units of PRBCs?



patient may need what if they're anticoagulated or on coummadin?

Vitamin K


PT positioning for systolic BP (will be on test)

patient is hypotensive, put them in supine or supine with legs elevated (head flat)


NG tube placement bright blood, coffee ground,no blood or bile, or bile no blood means for each?

-if you get bright blood on your NG placement, think upper GI
-coffee ground, upper GI but probably not active
-No blood and no bile, GI bleed is below the pyloric sphyncter
-bile but no blood, thinking no upper GI bleed at all


What does erythromycin do?

helps gastric motility to clear out stuff in upper GI so they can actually see what's happening


bowel prep to clean out bowel, most used?

go lightly



endoscopy: colonoscopy, sigmoidoscopy,
-injection therapy
-thermal coagulation therapy (light that causes coagulation)
-clip them



a mechanical blockage arising from a structural abnormality that presents a physical barrier to the progresssion of gut contents
-can be partial or complete, simple or strangulated



is a paralytic or functional variety of obstruction


patho of obstruction

results in
-initial overcoming of the obstruction by increased peristalsis
-increased intraluminal pressure by fluid and gas
-sequestration of fluid into the lumen from the surrounding circulation
-lymphatic and veous congestion resulting in oedematous tissue
-factors 3,4,5 result in hypovolaemia and electrolyte imbalance
-further: localized anoxia, mucosal depletion necrosis and perforation and peritonitis
-bacterial overgrowth with translocation of bateria and toxins causeing bacteraemia and septicaemia

What do we do?
-decomplress with NGT to low/intermittent suction
-replace lost fluid
-correction electrolyte abnormalities
-recognize strangulation and perforation (strangulation no passage of flatulance, severe pain, fever, peritoneal tenderness and swelling rigidity, leukocytosis, increases in amylase levels as well)
-systemic antibiotics


partial obstruction

classic sign, loose watery stool (passing around the blocking fecal matter)


a simple

obstruction that causes it to become ischemic


Small bowel adhesions

-accounts for 60-70% of all SBO
-results from peritoneal injury, platelet activation and givrin formation
-associated with starch covered gloves, intraperitoneal sepsis, haemorrhage and wash with irritant solutions iodine and other foreign bodies.
-As early as 4 weeks post laparotomy. The majority of patients present between 1-5 years
-70% of patients had a single band
-patient with complex bands are more likely to be readmitted
-readmission in surgically treated patients is 35%
-common surgeries you see them in: (25% colorectal surgery, 20% gynaecological, 14% in appendectomies)



-accounts for 20% SBO
-common: femoral, ID inguinal, umbilical, incisional and internal
-the site of obstruction is the neck of the hernia
-compromised viscus is with in the sac
-ischemia occurs initially by venous occlusion followed by edema and arterial compromise
-strangulation noted by: persistent pain, discoloration, tenderness, constitutional symptoms


Large Bowel obstruction

-distinguishing ileus from mechanical obstruction is challenging
-according to leplacs law: maximum pressure is at it's maximum diameter. CECUM is at the greatest risk of PERFORATION
-perforation resultes in release of feces with heavy bacterial contamination


Role of CT

-used with IV contrast, oral and rectal contrast (tripple contrast: IV, oral, and rectal contrast)
-able to demonstrate abnormallity in the bowel wall, mesentery, mesenteric vessels and peritoneum
-can show: level of obstruction, degree, causes, degree of ischemia, free fluid and gas


Barium bastrografin studies

-should not be used in pts with peritonitis
-used in acute abdomen but is diluted
-useful in recurrent and chronic obstruction


Initial dagnostics for LBO

-arterial blood gasses
-U& CRT, na, K Amylase, LFT and glucose, LDH
-group and save (x-match if needed)
-optional (ESR< CRP< Hepatitis profile)


ECG (cardiac ischemia)


Clinical finding BO high

-pain is rapid
-vomiting copiuous and contains bile jejunal content
-abdominal distention is limited or localized
-rapid dehydration from vomiting


Distal SBO

-pain: central and colicky
-vomitous is feculunt
-distension is severe
-visible peristalsis
-may continue to pass flatus and feacus before absolute constipation


Colonic BO

-? pre-existing change in bowel habit
-colicky in lower abdomen
-vomiting is late (has to back all the way up)
-distension prominent
-cecum ? distended


persistent pain may be a sign of



Clinical examination general, abdominal, and others

-vital signs, P, BP, Sat, RR, T
-anemia, jaundice, LN
-assessment of vomitus if possible
-full lung and heart exam

-abdominal distension and it's pattern
-hernial orifieces
-visible peristalsis
-cecal distention
-tenderness, guarding and rebound
-bowel sounds (high pitched, absent)
-rectal examination

-systemic examination
-if deemed necessary (CNS, vascular, gynecological, musculoskeletal)


Initial management of LBO

-resuscitate (60-100%), insert 2 lines, IVF (120ml and hour crystalloids), add K+ at 1mmmol/kg bc of vomiting (dropping K)
-draw blood
-inform senior member in team
-NPO, NG placement, urinary cath
-IV antibiotics
-If concern exist about fluid overloading a central line should be inserted
-follow-up lab results and correction of electrolyte imbalance
-pt should be nursed in intermediate care
-rectal tubes should only be used in Sigmoid volvulus


Indications for surgery

-Evidence of strangulation
-signs of peritonitis (bowel has ruptured)
-if the obstruction won't clear in 24-48 hours
-not sure why there is an obstruction or what is going on
-try to stabilize pt. before surgery



Associated with the following conditions:
-postop and bowel resection
-infection inside and outside the stomach
-spinal and pelvic fractures
-retro-peritoneal hematoma
-metabolic abnormalities
-bed ridden
-drug induced (morphine, tryciclic meds)


Ileus or obstruction?

Clinical features:
-is there an underlying cause?
-is the abdomen distended but tenderness is not marked
-is the bowel sounds diffusely hypoactive

Radiological features
-is the bowel diffusely distended
-is there gas in the rectum
-are further investigations helpful in showing an obstruction

Does the pt. improve on conservative measures?


Types of IAH/ACS primary, secondary, recurrent

-Primary: injury/disease of abdomino-pelvic region, "surgical"
-Secondary: sepsis, cap leak, burns, "medical"
-Recurrent: ACS develops despite surgical intervention


IAP interpretation

Pressure Interpretation
0-5 Normal
5-10 Common in most ICU pts
>12 (grade 1) Intra-abdominal HTN
16-20 (grade 2) Dangerous IAH- begin non- invasive intervention
>21-25 (grade 3) Impending, decompressive lappi



ischemia leads to inflammatory responses, cap leakage, coupled with our fluid resuscitation, tissue edema, increases abd pressure, leads back to more ischemia creating this cycle


causes of IAP elevation and findings

-major abdominal/retroperitoneal problem
-ischemic insult/SIRS requiring fluid resuscitation with a positive fluid balance of 5 OR MORE LITERS within 24 HOURS (10lb weight gain)

-temp, HR, and resp increases, WBC .12,000 (elevates)


physiologic sequelae cardiac

-increased ABD pressure cause compression of vena cava with reduced venous return
-elevated intra-thoracic pressure with multiple negative cardiac effects

-decreased cardiac output, increased SVR
-increased cardiac work loads
-decreased tissue perfusion
-misleading elevations of CVP and PAWP
-cardiac insufficiency, cardiac arrest


physiologic sequalae pulmonary

incrased intra-abd pressure casuses
-elevated diaphragm, reduced lung bolumes and alveolar inflation, stiff thoracic cage, increased intersitial fluid

-elevated intrathoracic pressure
-incread peak pressure, reduced tidal volumes
-Barotrauma-atelectasis, hypoxia, hypercarbia


physiologic sequalae gastrointestinal

increased intra abd pressure causes
-compression and congestion of mesenteric veins and capillaries
-reduced cardiac output to the gut

-decreaes gut perfusion incresaed gut edema and leak
-ischemia, necrosis
-bacterial translocation
-development and perpetuation of SIRS
-further increase in IAP


physiologic renal

elevated IAP causes
-compression of renal veins, parenchyma
-resuced cardiac output to kidneys

-reduced BF to kidney
-renal congestion and edema
-dereaed glomerular filtration
-renal failure, oliguria/anuria


physiologic neuro

elevated IAP causes
-increased intrathoracic pressure
-increases in superior vena cava pressure with reduction in drainage of SVC into the thorax

increaed central venous pressure and IJ pressure
-increased ICP
-decreaed CPF
-cerebral edema, brain anoxia, brain injury



abdominal perfusion pressure = MAP-IAP
-reflects actual gut perfusion bettter than IAP alone
-optimizing APP.60 mm HG should probably be primary endpoint


Decompressive laparotmy

-delay in abd compression may lead to intestinal ischemia, decompress early


bladder pressure monitoring how to?

insert catheter to bladder, hook to transducer, read pressures off of the bladder
-make sure transducer is level with the bladder


patient meets one of the following criteria and has at least two risk factor for IAH:

-new intensive care until admission
-evidence of clinical deterioration or new organ failure

risk factors:
-Diminished abd wall compliance
-increased intraluminal contents
-increased abdominal contents
-capillary leak/fluid resuscitation


how you messure

-messure in expiration, pt. laying supine
-put in 25 ml fluid to measure it against
-wait 30 seconds and measure it